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疹病毒降低了非经典抗原呈现分子CD1d的表达

Renee Traves¹, Tara Opadchy¹, Barry Slobedman¹

¹Infection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, Charles Perkins Centre, University of Sydney, New South Wales, Australia.

The Journal of infectious diseases

|November 16, 2023

概括

疹病毒 (VZV) 感染降低了CD1d分子的表达,影响了不变的自然杀手T (iNKT) 细胞反应. 这种VZV对CD1d-iNKT轴的操纵对于理解病毒病原性至关重要.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
分子生物学分子生物学

背景情况:

CD1d分子向不变的自然杀手T (iNKT) 细胞呈现脂质抗原,弥合先天性和适应性免疫.
通过CD1d激活iNKT细胞对于免疫反应至关重要,特别是在像疹病毒 (VZV) 这样的病毒感染中.
CD1d或iNKT细胞的缺陷与严重的VZV感染有关,突出显示了它们的保护作用.

研究的目的:

研究VZV感染对CD1d表达和功能的影响.
阐明VZV调节CD1d-iNKT细胞轴的机制.

主要方法:

尤尔卡特细胞感染了三个VZV菌株 (VZV-S,rOka,VZVrOka-66S).
流细胞计评估了受感染和未受感染细胞中的CD1d蛋白水平.
反转录聚合酶连锁反应分析了CD1d转录水平.
共同培养实验探讨了可溶性因素和细胞接触的作用.

主要成果:

在感染细胞和抗原阴性细胞上,VZV显著降低了CD1d蛋白的调节.
CD1d下调取决于细胞间接触.
发现VZV的向是CD1d的转录.
病毒激酶ORF66与感染细胞中的CD1d调节有关.

结论:

VZV采用多种策略来降低CD1d转录和蛋白质的下调.
这些发现证明了VZV对CD1d-iNKT细胞免疫路径的积极操纵.
这种操纵可能有助于VZV病变和免疫逃避.

关键词:

CD1d 是一个CD1d.VZVVVVVVVZVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV 免疫调节的免疫调节疹病毒 (varicella zoster virus) 是一种病毒.

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